The hypothesis is that keratinocyte growth factor (KGF) and laminin together with telomerase direct the fate of AEC between proliferation, differentiation, and/or apoptosis both during lung development and repair after lung injury through tyrosine phosphorylation cascades targeting cyclin D and retinoblastoma protein (pRb). Characterization of the molecular signaling mechanisms determining the proliferative versus apoptotic versus differentiated "survival" fate of AEC will identify new targets for the design of novel rational therapeutic approaches to amelioration of alveolar injury and augmentation of repair in both neonatal and adult human alveolar injury.